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Immunohistochemical study on the expression of calcium binding proteins (calbindin-D28k, calretinin, and parvalbumin) in the cerebral cortex and in the hippocampal region of nNOS knock-out(-/-) mice

  • Cho, Yu-Jin (Department of Anatomy, College of Medicine, Seoul National University) ;
  • Lee, Jae-Chul (Department of Anatomy, College of Medicine, Seoul National University) ;
  • Kang, Bong-Gu (Department of Anatomy, College of Medicine, Seoul National University) ;
  • An, Jae-Yeol (Department of Anatomy, College of Medicine, Seoul National University) ;
  • Song, Hyeon-Suk (Department of Anatomy, College of Medicine, Seoul National University) ;
  • Son, On-Ju (Department of Anatomy, College of Medicine, Seoul National University) ;
  • Nam, Do-Hyun (Department of Neurosurgery, School of Medicine, Sungkyunkwan University) ;
  • Cha, Choong-Ik (Department of Anatomy, College of Medicine, Seoul National University) ;
  • Joo, Kyeung-Min (Department of Anatomy, College of Medicine, Seoul National University)
  • Published : 2011.06.30

Abstract

Nitric oxide (NO) modulates the activities of various channels and receptors to participate in the regulation of neuronal intracellular $Ca^{2+}$ levels. $Ca^{2+}$ binding protein (CaBP) expression may also be altered by NO. Accordingly, we examined expression changes in calbindin-D28k, calretinin, and parvalbumin in the cerebral cortex and hippocampal region of neuronal NO synthase knockout(-/-) ($nNOS^{-/-}$) mice using immunohistochemistry. For the first time, we demonstrate that the expression of CaBPs is specifi cally altered in the cerebral cortex and hippocampal region of $nNOS^{-/-}$ mice and that their expression changed according to neuronal type. As changes in CaBP expression can infl uence temporal and spatial intracellular $Ca^{2+}$ levels, it appears that NO may be involved in various functions, such as modulating neuronal $Ca^{2+}$ homeostasis, regulating synaptic transmission, and neuroprotection, by influencing the expression of CaBPs. Therefore, these results suggest another mechanism by which NO participates in the regulation of neuronal $Ca^{2+}$ homeostasis. However, the exact mechanisms of this regulation and its functional significance require further investigation.

Keywords

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